Selective cortical interneuron and GABA deficits in cyclin D2-null mice
Open accessAbstract
In contrast to cyclin D1 nulls (cD1-/-), mice without cyclin D2 (cD2-/-) lack cerebellar stellate interneurons; the reason for this is unknown. In the present study in cortex, we found a disproportionate loss of parvalbumin (PV) interneurons in cD2-/- mice. This selective reduction in PV subtypes was associated with reduced frequency of GABA-mediated inhibitory postsynaptic currents in pyramidal neurons, as measured by voltage-clamp recordings, and increased cortical sharp activity in the EEGs of awake-behaving cD2-/- mice. Cell cycle regulation was examined in the medial ganglionic eminence (MGE), the major source of PV interneurons in mouse brain, and differences between cD2-/- and cD1-/- suggested that cD2 promotes subventricular zone (SVZ) divisions, exerting a stronger inhibitory influence on the p27 Cdk-inhibitor (Cdkn1b) to delay cell cycle exit of progenitors. We propose that cD2 promotes transit-amplifying divisions in the SVZ and that these ensure proper output of at least a subset of PV interneurons.
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Nr2f1 and Nr2f2 influence neuronal specification by regulating cell cycle dynamics, which may explain why cell cycle factors have been implicated in interneuron diversity.
“Nr2f1 and Nr2f2 influence neuronal specification by regulating cell cycle dynamics”
From Development and Functional Diversification of Cortical Interneurons (2018) · cites this paper as Glickstein et al., 2007
Loss of cyclin D2 results in a 30-40% reduction in PV-expressing neocortical interneurons with no change in SST interneuron numbers.
“loss of the cell cycle regulator cyclin D2, which is enriched within SVZ BPs of the MGE, results in a 30–40% reduction in PV-expressing neocortical interneurons with no change in SST interneuron numbers”
From Hippocampal GABAergic Inhibitory Interneurons (2017) · cites this paper as [406]
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- Authors
- Glickstein, S. B., Moore, H., Slowinska, B., Racchumi, J., Suh, M., Chuhma, N., & Ross, M. E.
- Affiliations
- Weill Cornell Medicine (US)
- New York State Psychiatric Institute (US)
- Venue
- Development
- Publisher
- The Company of Biologists
- Published
- 2007-11-15
- Volume
- 134
- Issue
- 22
- Pages
- 4083-4093
- ISSN
- 0950-1991 (ISSN-L)
- 1477-9129
- PMC
- PMC3396210
- OpenAlex
- W2160291365
- Cited by
- 89
- References
- 44
- Citations by year
- 2025: 2 · 2024: 3 · 2023: 4 · 2022: 3 · 2021: 4 · 2020: 7 · 2019: 4 · 2018: 6 · 2017: 12 · 2016: 4 · 2015: 9 · 2014: 5 · 2013: 4 · 2012: 2
- FWCI
- 1.13
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Development (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (P01NS048120)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- cyclin D2, cyclin D1, parvalbumin interneurons, cortical interneurons, GABAergic inhibition, inhibitory postsynaptic currents, medial ganglionic eminence, subventricular zone, cell cycle regulation, p27, interneuron migration
- MeSH terms
- Animals, Cell Cycle, Cerebral Cortex, Female, gamma-Aminobutyric Acid, Interneurons, Male, Mice, Inbred C57BL, Models, Biological, Organ Specificity, Parvalbumins, Pregnancy, Synapses, Cyclins, Mice, Knockout, Genes, bcl-1, Mice, Cyclin D2
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